module 4: intracranial regulation

Components of CNS

-brain

-spinal cord

-cranial nerves

-autonomic nervous system

-sympathetic nervous system

-parasympathetic nervous system

Hydantoins administration

-Give with meals

-IV use – monitor for CV collapse if given too quickly

-No more than 50 mg/min, in older adults no more than 25mg/min

-Therapeutic range is very narrow 10-20mcg/mL.

Serotonin agonists administration

Admin: oral, nasal spray, SQ injection

-SQ give once and repeat in one hour. No more than two SQ doses in 24-hour period.

-Give one oral tablet and repeat once after 2 hours if there’s no relief. No more than 200 mg in a 24 hour period

MAO-B administration

-oral disintegrating form on top of the tongue and refrain from eating or drinking for 5 minutes before or after administration

-Give before the morning meal.

-Do NOT give after noon

Direct acting dopamine receptor agonists administration

-Begin with small dose and increase it every 5-7 days

-If for restless leg syndrome, give it 2-3 hours before bedtime to allow for therapeutic effects

Dopaminergic agents administration

-Begin low dose and gradually increase

-6 months to achieve the full therapeutic response

-IR tablets begin working within 30 minutes ER over 4-6 hours can take up to 2 hours to begin working in morning.

Brain

-covered by meninges

-responsible for sending, receiving, and processing information related to sensation, movement, communication, memory, emotions, and thought processing

-Contains cerebrum, cerebellum, brainstem

Cerebrum

Largest structure of the brain

Cerebellum

-Contains 80% of all neurons

-Receive immediate and continuous information about the condition of the muscles, joints, and tendons

Cranial nerves

12 pairs

Sympathetic nervous system

-Cells originate in the gray matter of the thoracolumbar region of the spinal cord

-“Fight or flight”

Parasympathetic nervous system

-Originate in the gray matter of the sacral area of the

spinal cord

-Typically, not under conscious control

-Cells originate in the gray matter of spine

-Rest and Digest

Glasgow coma scale

Eye opening (4)

Motor response (6)

Verbal response (5)

Eye opening scale

4 = spontaneous

3 = to sound

2 = to pain

1 = never

Motor response scale

6 = obeys commands

5 = localizes pain

4 = normal flexion (withdrawal)

3 = abnormal flexion

2 = extension

1 = none

Verbal response scale

5 = oriented

4 = confused conversation

3 = inappropriate words

2 = incomprehensible sounds

1 = none

Parkinson’s Disease

-Idiopathic, chronic, progressive degenerative disorder of CNS

-Has motor, nonmotor, neuropsychiatric manifestations

-Affects individuals over age 50

-Second most common neurodegenerative disorder

4 cardinal Parkinson’s symptoms

-Tremors

-Bradykinesia

-Rigidity

-Postural instability

Primary parkinsonism

Situation in which symptoms occur due to Parkinson disease

Secondary parkinsonism

Situation in which these symptoms occur due to some cause other than Parkinson disease

Pathophysiology of parkinsons

-Motor activity occurs as a result of integrating the actions of the cerebral cortex, basal ganglia, and cerebellum

-The secretion of dopamine and acetylcholine in the body produce inhibitory and excitatory effects on the muscles respectively.

-Overstimulation of the basal ganglia by acetylcholine occurs because degeneration of the substantia nigra results in decreased dopamine production. This allows acetylcholine to dominate, making smooth, controlled movements difficult.

-Treatment of PD focuses on increasing the amount of dopamine or decreasing the amount of acetylcholine in a client’s brain.

-70-80% deficiency in order to demonstrate manifestations of PD

Causes of parkinsons

-Idiopathic (90%)

-Genetic (10%)

Parkinsons increased risk factors

-Increased age (most significant over the age of 50)

-Male gender at birth

-Exposure to pesticides, metals, other compounds

-Family history of PD

-Genetic mutations

Parkinsons decreased risk

-Cigarette smoking, caffeine intake

-High blood urate levels

Parkinson clinical manifestations

-Insidious onset

-Motor features

-Tremor

-“Pill-rolling” resting tremor of hand

-Tremor of lips, chin, jaw, tongue, legs

-Rigidity from increased muscle stiffness and tone

-Gait Shuffling

-Cogwheeling

-Bradykinesia

-Postural instability

Parkinson nonmotor manifestations

-Fatigue, sleep disturbances

-Olfactory dysfunction

-Pain

-Autonomic dysfunction

-Orthostatic hypotension, drooling, nocturia

Neuropsychiatric symptoms

-Cognitive dysfunction, dementia, psychosis, hallucinations

-Mood disorders, depression, anxiety

Stage I

Unilateral shaking or tremor of one limb

Stage II

-Bilateral limb involvement occurs, making walking and balance difficult

-Masklike face

-Slow, shuffling gait

Stage III

-Physical movements slow down significantly, affecting walking more

-Postural instability

Stage IV

Tremors can decrease but akinesia and rigidity make day-to-day tasks difficult

Stage V

-Client unable to stand or walk

-dependent for all care

-might exhibit dementia

Nonsurgical management of parkinson

-drug therapy, exercise programs, or physical therapy

-Allow the patient extra time to answer questions

-Monitor for side effects of medications

-Allow patient time to provide ADLs and mobility

-Schedule appointments that are at the patient’s optimal time

-Speak slowly and clearly

-Monitor the eating and swallowing

-Assess for depression, anxiety, and impaired cognition

Parkinson treatments

-Medication

-Deep brain stimulation – decreases tremors and involuntary movements

-Complementary and supportive therapies

Parkinson medications

-Dopamine agonists

-Anticholinergic agents

-Amantadine

-Monoamine oxidase inhibitors

-Catechol-O-methyltransferase inhibitors

Dopamine replacement drugs/dopaminergic agents

Levodopa, carbidopa

Dopaminergic agents MOA

-Cross blood-brain barrier, then taken up by the remaining dopaminergic neurons in the substantia nigra

-medication is converted to dopamine in theses neurons and is available for use

Dopaminergic agents therapeutic use

-Parkinson’s, but diminish by year 5

-“Wearing off” times can occur, at end of cycle or anytime

Dopaminergic agents adverse effects

-Nausea and vomiting, drowsiness

-Dyskinesias – during initial phase of treatment or inappropriate dosing

-Orthostatic Hypotension

Dopaminergic agents contraindications

-Angle-closure glaucoma

-History of melanoma, psychosis, or suicidal thoughts.

-Caution: renal, hepatic, respiratory, endocrine disorders, wide-angle glaucoma, PUD, or depression or bipolar disorder

Dopaminergic agents interactions

-Haloperidol and chlorpromazine and vitamin B6 supplements decrease the action of levodopa/carbidopa

-Anticholinergics increase a client’s response to levodopa/carbidopa because they alter the balance between dopamine and acetylcholine in the brain by blocking the release of acetylcholine

-MAOis within the past two weeks – HTN crisis

Dopaminergic agents nursing considerations

-Monitor for dyskinesia – decrease dosage may be needed. Amantadine can be used to treat

-Monitor for falls/hypotension

-Take with food, but avoid high-protein foods as they decrease the absorption

-Urine and sweat may darken

Direct acting dopamine receptor agonists

Bromocriptine, pramipexole, ropinirole

Direct acting dopamine receptor agonists MOA

-Bind to dopamine receptors and causing a response similar to the body’s natural dopamine

-These drugs mimic the chemical dopamine in the body

Direct acting dopamine receptor agonists therapeutic uses

-Parkinson’s, but diminish by year 5

-Restless Leg Syndrome

-Used in late stages to decrease levodopa/carbidopa usage and fluctuations

Direct acting dopamine receptor agonists adverse effects

-Nausea and other GI symptoms

-Orthostatic Hypotension

-Dyskinesia

-Daytime sleepiness – “sleep attacks”

-Muscle weakness

Direct acting dopamine receptor agonists contraindications

-Major psychotic disorder, renal dysfunction, or liver dysfunction.

-Caution in older adults, pregnancy, and lactation

Direct acting dopamine receptor agonists interactions

-Cimetidine – increased levels

-Metoclopramide – decreases the therapeutic effects

-Phenothiazine antipsychotics – decrease the effect

-Alcohol and CNS depressants increase risk for adverse effects

Direct acting dopamine receptor agonists nursing considerations

-Take with food

-Monitor for drowsiness or sudden episodes of extreme sleepiness and move clients to a safe environment.

-Monitor muscle weakness for falls

-Monitor VS for orthostatic hypotension

-Adm

-Taper discontinuation over 1 week period

Monoamine oxidase-B (MAO-B)

Selegiline, rasagiline

MAO-B MOA

-Indirect-acting dopamine receptor agonists inhibit the action of the enzyme monoamine oxidase B in the brain and other parts of the body

-Inactivates several chemical neurotransmitters

-MAO-A: inactivates epinephrine and norepinephrine

-MAO-B inactivates dopamine.

MAO-B therapeutic uses

-Parkinson’s disease

-Adjunct to levodopa/carbidopa

MAO-B adverse effects

-Insomnia

-Hypertensive crisis – Tyramine and other medications

-Oral mucous membrane irritation.

MAO-B contraindications

-PUD

-Hypersensitivity to MAO-B inhibitors

MAO-B interactions

-Meperidine, opioids, MAOIs, tricyclic antidepressants, and SSRI can cause high fever and muscle rigidity.

-Foods with tyramine or herbals (St. John’s wort, ginseng, or ma Huang,) may cause severe HTN

-Antihypertensive drugs, diuretics, and general anesthetics may cause hypotension

MAO-B nursing considerations

-Monitor for insomnia and BP

-Monitor and educate on foods high in tyramine or caffeine

Anticholinergics

-benztropine and trihexyphenidyl

-help control tremors and rigidity

Anticholinergics nursing actions

Monitor for anticholinergic effects (dry mouth, constipation, urinary retention, acute confusion)

Catechol O-methyltransferase (COMT) inhibitors

-entacapone

-decrease the breakdown of levodopa, making more available to the brain as dopamine

-can be used in conjunction with a dopaminergic and dopamine agonist for better results

COMT inhibitors nursing actions

-Monitor for dyskinesia/hyperkinesia when used with levodopa.

-Assess for diarrhea.

-Dark urine is a normal finding

Migraine

-Recurrent, episodic attacks of head pain often with nausea, sensitivity to light or sound or head movement

-Stress and Anxiety

-Throbbing, unilateral often behind one eye or ear

-Can last 4-72 hours

-Familial, Women at birth more than men

-Higher risk for stroke and epilepsy

Migraine health promotion and disease prevention

-Promote stress management strategies and recognition of triggers of the onset of a headache

-Recommend use of a headache diary to help identify type of headache and response to interventions

-Promote hand hygiene to prevent the spread of viruses that produce manifestations like the common cold

-Review pain management to include over-the- counter medications and herbal remedies

-Review risk factors (triggers) for both migraine and cluster headaches

Possible triggers for migraine headaches

-Alcohol or environmental allergies

-Intense odors, bright lights, overuse of some medications

-Fatigue, sleep deprivation, depression, emotional or physical

stress, anxiety

-Hormone fluctuations associated with menstrual cycles and oral contraceptive use

-Foods containing tyramine, nitrites, or dairy

Causes of migraines

-Neuronal hyperexcitability

-Calcitonin gene-related peptide or CGRP rise during the migraine, while levels of 5- hydroxy-tryptamine, or 5-HT, fall.

-Vascular: Sterile brain tissue inflammation

-Genetic

-Sodium-potassium pump channels

-Serotonin and dopamine receptors

-Hormonal

-Environmental factors

-Caffeine, red wine, and MSG

-Light-sensitivity, stress, excessive fatigue, or change in weather

Migraine with aura prodromal phase

-Hours to Days

-Irritability, depression, food cravings

-Diarrhea/constipation

-Frequent Urination

Migraine with aura aura phase

-about 1 hour prior

-Numbness and tingling of the mouth, lips, face or hands

-Acute confusion

-Visual disturbances – light flashes and bright spots

Migraine with aura second phase

-HA - Severe, incapacitating intensifies over several hours

-Nausea, vomiting

-Drowsiness and vertigo

Migraine with aura third phase

-Pain changes from throbbing to dull

-HA, N/V lasting 4-72 hours

Migraine with aura recovery

-Muscle aches and contraction of head and neck muscles ar common

-Physical activity worsens pain

-Sleep

Migraine without aura

-Migraine beginning without an aura before the onset of the HA

-Pain aggravated by performing physical activities

-Pain that is unilateral and pulsating

-One of these symptoms is present

-N/V

-Photophobia

-Phonophobia

-HA 4-72 hours

-Often early in the morning, during periods of stress, or premenstrual tensions

Migraine preventive therapy

-NSAID

-BB – Propranolol and timolol

-Chronic Migraine Treatment

-Ona botulinum toxin A

-HA Diary

-Avoiding Tyramine-containing products

-Cool/dark environment

-Get rest and sleep

-Avoid intense odors

Migraine abortive therapy

-Alleviating pain during the aura phase

-APAP or NSAIDs

-Caffeine combination

-Antiemetics – for nausea

-Triptan preparations,

-Activates 5-HT (Serotonin) receptors to cause vasoconstriction

-Ergotamine derivatives (Ergot Alkaloids)

-Promote constriction of cerebral blood vessels

-Isometheptene in combinations formulations

Cluster headaches risk factors

-More frequent during spring and fall

-More common in males (sex assigned at birth) between 20 to 50 years of age

Cluster headaches expected findings

-Brief episode of intense, unilateral, nonthrobbing pain lasting 15 min to 3 hrthat can radiate to forehead, temple, or cheek

     -Occurring daily 1 to 8 times daily

     -Followed by period of remission

-No aura or preliminary manifestations

-Less common than migraines

-Tearing of the eye with runny nose and nasal congestion

-Facial sweating

-Drooping eyelid and eyelid edema

-Miosis (pupil constriction)

-Facial pallor or flushing

-Bradycardia

-Nausea and vomiting

-Pacing, walking, or sitting and rocking activities

Cluster headaches medications

-Triptans

-Ergotamine preparations

-Antiepileptic medications

-Calcium channel blockers

-Corticosteroids

-Over-the-counter capsaicin

-Melatonin

-Glucosamine

Oxygen therapy for cluster headaches

12L/Min for 15-20 minutes at the onset of HA

Serotonin agonists

Sumatriptan, zolmitriptan

Serotonin agonists MOA

-Reversing the 5-HT/CGRP ratio

-Activates 5-HT receptors, which promote vasoconstriction and suppress the release of CGRP reducing inflammation

Serotonin agonists therapeutic uses

-Migraine

-Cluster headache

Serotonin agonists adverse effects

-Chest pressure or “heaviness”

-CNS – tingling sensation and vertigo

Serotonin agonists contraindications

-CAD, angina, or previous MI.

-PAD or CVA.

-Caution in liver or kidney disease

Serotonin agonists interactions

-MAOIs within 2 weeks.

-Use of another triptan within 24 hours increases angina.

-SSRIs – serotonin syndrome

-St. John’s wort may cause sumatriptan toxicity

Serotonin agonists nursing considerations

Monitor vital signs closely after the first dose

Migraine non-med interventions

-Medical marijuana

-External trigeminal nerve stimulator

-Complimentary and integrative health

Seizure activity

-Abnormal electrical discharges within brain

-Results in involuntary movement and/or behavior and sensory alterations

-Involuntary movements may encompass entire body or just certain muscle groups

-Changes in level of consciousness, behavior, or sensory perception

Epilepsy

term used to define chronic recurring abnormal brain electrical activity resulting in two or more seizures

Seizure risk factors

-Genetic predisposition

-Acute febrile state

-Head trauma

-Cerebral edema

-Exposure to toxins

-Infection

-Abrupt cessation of antiepileptic drugs (AEDs)

-Stroke

-Heart disease

-benign, seizures caused by the increased bulk associated with the tumor

-Hypoxia

-Hormonal

-Fluid and electrolyte imbalances

-Acute substance withdrawal

Tonic clonic seizures

Lasting 2-5 minutes begins with stiffening or rigidity of the muscles and immediate LOC

Tonic seizures

-Only the tonic phase is experienced

-LOC, Sudden increased muscle tone, and autonomic manifestations (arrythmia, apnea, vomiting, incontinence)

-Last less than 30 seconds

Clonic seizures

-Only the clonic phase of rhythmic jerking of extremities is experienced

-Lasts several minutes

Myoclonic seizures

-Brief jerking or stiffening of the extremities that may occur singly or in groups

-Lasts only for seconds

Atonic (akinetic) seizures

Sudden loss of muscle tone, lasting for seconds, followed by postictal confusion

Absence seizures

-LOC for 10-30 seconds

-No motor activity

-May occur several hundred times daily

-Typical in adolescents

Partial (local or focal) seizures

Begin in one part of the cerebral hemisphere

Complex partial (psychomotor or temporal lobe)

-May case LOC

-Automatisms – lip smacking or picking at clothes

Simple partial seizures

-Consciousness is maintained

-Unusual sensations, sense of déjà vu, unilateral abnormal extremity movements, offensive smell

Tonic phase

-15-60 seconds

-Muscular rigidity

-Sudden loss of consciousness

-Pupils fixed and dilated

-Increased metabolic demands

-Hypoxia

-Skin pallor and cyanosis (r/t cyanosis)

-Urinary and bowel incontinence

Clonic phase

-(60–90 seconds)

-Alternating muscular contraction and relaxation in extremities

-Hyperventilation

-Eyes roll back, froth at mouth

Postictal period

-Decreased level of consciousness; sleepy

-Quiet and relaxed breathing

-Gradual regaining of consciousness

Seizure disorder diagnostics

-Labs

-EEG

-Lead level, toxicology screening

-CT scan or MRI and angiography

Seizure disorders labs

-Complete blood cell count

-Blood chemistry

-Urine culture

-Lumbar puncture